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Resistance to transforming growth factor beta-mediated tumor suppression in melanoma: are multiple mechanisms in place?Lasfar A; Cohen-Solal KACarcinogenesis 2010[Oct]; 31 (10): 1710-7Resistance to transforming growth factor (TGF) beta-mediated tumor suppression in melanoma appears to be a crucial step in tumor aggressiveness since it is usually coupled with the ability of TGFbeta to drive the oncogenic process via autocrine and paracrine effects. In this review, we will focus mainly on the mechanisms of escape from TGFbeta-induced cell cycle arrest because the mechanisms of resistance to TGFbeta-mediated apoptosis are still essentially speculative. As expected, some of these mechanisms can directly affect the function of the main downstream effectors of TGFbeta, Smad2 and Smad3, resulting in compromised Smad-mediated antiproliferative activity. Other mechanisms can counteract or overcome TGFbeta-mediated cell cycle arrest independently of the Smads. In melanoma, some models of resistance to TGFbeta have been suggested and will be described. In addition, we propose additional models of resistance taking into consideration the information available on the dysregulation of fundamental cellular effectors and signaling pathways in melanoma.|Apoptosis[MESH]|Cell Cycle[MESH]|Contractile Proteins/physiology[MESH]|Cyclin-Dependent Kinase 4/metabolism[MESH]|Cyclin-Dependent Kinase Inhibitor p21/analysis[MESH]|Disease Progression[MESH]|Filamins[MESH]|Forkhead Box Protein O1[MESH]|Forkhead Transcription Factors/physiology[MESH]|Genes, myc[MESH]|Humans[MESH]|Intracellular Signaling Peptides and Proteins/physiology[MESH]|Melanoma/*pathology/prevention & control[MESH]|Microfilament Proteins/physiology[MESH]|PAX3 Transcription Factor[MESH]|Paired Box Transcription Factors/physiology[MESH]|Phosphorylation[MESH]|Proto-Oncogene Proteins/physiology[MESH]|Signal Transduction[MESH]|Smad2 Protein/physiology[MESH]|Smad3 Protein/physiology[MESH]|Transforming Growth Factor beta/*physiology[MESH] |
